The Physiology of eating disorders

Abstract

This article summarizes current understanding of the pathophysiology of anorexia nervosa. Evidence is reviewed of alterations in hypothalamic‐pitui‐tary‐thyroid mechanisms, catecholamine metabolism, and endogenous opioid activity. It is concluded that once weight loss and starvation occur, the usual mechanisms for release and inhibition of various regulators of eating behavior change, and a new set of regulating mechanisms is instituted. Thus, despite an increased body of knowledge, understanding of the origins of anorexia nervosa still eludes us.

Do eating disorders and affective disorders share a common etiology? A dissenting opinion

“…That the HPA axis is disrupted both in anorexia nervosa and affective disorders is well known. Findings common to both include increased cortisol secretion, inadequate suppression of cortisol by dexamethasone, a blunting of ACT'H response to corticotropin releasing hormone (CRH), and increased levels of CRH in spinal fluid (for reviews see Hudson & Hudson, 1984;Hudson & Pope, in press;Strober & Katz, in press;Weiner, 1985). Frequency of dexamethasone nonsuppression is also increased in bulimic patients as well, but 24 hour levels of cortisol secretion are normal (Gold et al, 1986;Hudson et al, in press;Walsh et al, in press).…”

“…Conversely, unlike the general pattern in anorexic patients, HPA abnormalities in primary depression fluctuate in closer synchrony with the onset and offset of episodes, although weight loss can be a contributing factor in some patients (Casper et al, in press). As far as catecholamine metabolism is concerned, plasma, urine, and s p u d fluid amine concentrations are generally decreased in underweight anorexic patients and revert to normal when weight is corrected (Garfinkel & Gamer, 1982;Weiner, 1985), although persistence of low levels of norepinephrine in plasma and CSF has been reported in some long-term weight recovered patients (Kaye et al, 1985). In contrast, the available data on endogenously depressed patients suggest that levels of norepinephrine are higher and sigruficantly more variable than in controls (Roy et al, 1985;Siever et al, 1986), suggesting activation or dysregulation of noradrenergic mechanisms.…”

Life stress, psychological symptoms and weight reducing behavior in adolescent girls: A prospective analysis

“…In addition, daily life stressors are likely to be increased in weight reducers who need to alter their lifestyles in order to adhere to dieting (e.g., going out less with friends in order to avoid eating). From the biological perspective on anorexia nervosa, it has been hypothesized that mood and cognitive disturbances are attributable to the neuroendocrine alterations that accompany starvation (Garfinkel & Kaplan, 1985;Weiner, 1985). It is possible that less extreme forms of undernourishment could cause negative cognitive/affective changes in the adolescent dieter as well.…”

Annotation: Eating Disorders in Children

“…Possibilities include immaturity, damage or dysfunction in the hypothalamic centres regulating eating and reproduction, anomalous neuronal connections in the hypothalamus, or abnormalities at receptor sites. Weiner (1985) has proposed that hypothalamic tissue may be abnormally sensitive in some individuals, and that in times of stress dysfunction is triggered. Once a specific abnormality has been identified it should be possible to determine whether this is primary or secondary.…”